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目的:研究急性运动或AICAR注射对mTOR及下游信号的影响,旨在探讨AMPK调控骨骼肌蛋白合成的机制。方法:52只雄性SD大鼠分为4组:安静对照组(n=8)、运动组(n=18)、生理盐水注射对照组(n=8)、AICAR注射组(n=18)。运动速度26 m/min,坡度10%,时间60 min。运动和注射组分别在结束后即刻、1h、6 h和1 h2、h6、h取材。结果:运动后即刻、注射后1 h,mTOR Ser2448磷酸化(分别下降45%和38%)和4E-BP1 Thr37/46磷酸化均显著降低(分别下降34%和38%),运动后1 h和注射后2 h mTOR及4E-BP1开始增加,6 h达峰值。注射组S6K1 Thr389磷酸化水平在各时间点无显著变化,运动组均显著升高(分别增加42%、52%和57%)。结论:一次性剧烈运动或AICAR注射导致蛋白合成的暂时抑制,其机制与AMPK下调mTORSer2 448及其下游信号4E-BP1 Thr37/46的磷酸化水平有关,但未发现S6K1 Thr389磷酸化水平的下调。
OBJECTIVE: To study the effects of acute exercise or AICAR injection on mTOR and downstream signaling in order to explore the mechanism of AMPK regulating skeletal muscle protein synthesis. Methods: 52 male SD rats were divided into 4 groups: control group (n = 8), exercise group (n = 18), saline injection control group (n = 8) and AICAR injection group (n = 18). Movement speed 26 m / min, gradient 10%, time 60 min. Exercise and injection groups were immediately after the end, 1h, 6h and 1h2, h6, h drawn. RESULTS: Phosphorylation of mTOR Ser2448 (45% and 38% decrease) and 4E-BP1 Thr37 / 46 phosphorylation were significantly reduced (34% and 38% decrease, respectively) immediately after exercise and 1 h after injection At 2 h after injection, mTOR and 4E-BP1 began to increase, reaching the peak at 6 h. The phosphorylation level of S6K1 Thr389 in injection group did not change significantly at all time points, and the exercise group was significantly increased (42%, 52% and 57% respectively). CONCLUSION: One-time strenuous exercise or AICAR injection results in a temporary inhibition of protein synthesis. The mechanism is related to AMPK down-regulation of phosphorylation of mTORSer2 448 and its downstream signal 4E-BP1 Thr37 / 46, but no down-regulation of S6K1 Thr389 phosphorylation is found.